Hisako Endo1, Tamiko Takemura2, Masashi Fukayama3, Osamu Tsutsumi4. 1. Department of Pathology, University of Tokyo Hospital. 2. Department of Pathology, Japanese Red Cross Medical Center. 3. Department of Pathology, Graduate School of Medicine, University of Tokyo. 4. Department of Obstetrics and Gynecology, University of Tokyo Hospital, Tokyo, Japan.
Abstract
Background: Studies in several countries have reported a decline in human sperm quality similar to that observed in wild animals. To quantify whether the number of sperm in humans has decreased and whether humans are affected by similar environmental influences, we compared the number of spermatogonia and Sertoli cells in human fetal and neonatal testes autopsied at two institutions in Tokyo between 1958-1964 (term A) and 1989-1998 (term B), with special attention to chronological changes during gestation. Methods: We used an immunohistochemical method with antibody against neuron-specific enolase to determine the percentage of seminiferous tubules containing spermatogonia in the formalin-fixed tissue samples, and a morphometrical method using a dissector to count the number of spermatogonia. Results: There were no significant statistical differences between the two time periods in the regression parameters compared for the number of spermatogonia and Sertoli cells, nor was there a remarkable difference in the estimated number of Leydig cells. Conclusion: The results indicate that even if there has been a deterioration in human semen quality, it is not necessarily caused by endocrine disruption of fetal testicular development. (Reprod Med Biol 2006; 5: 65-70).
Background: Studies in several countries have reported a decline in human sperm quality similar to that observed in wild animals. To quantify whether the number of sperm in humans has decreased and whether humans are affected by similar environmental influences, we compared the number of spermatogonia and Sertoli cells in human fetal and neonatal testes autopsied at two institutions in Tokyo between 1958-1964 (term A) and 1989-1998 (term B), with special attention to chronological changes during gestation. Methods: We used an immunohistochemical method with antibody against neuron-specific enolase to determine the percentage of seminiferous tubules containing spermatogonia in the formalin-fixed tissue samples, and a morphometrical method using a dissector to count the number of spermatogonia. Results: There were no significant statistical differences between the two time periods in the regression parameters compared for the number of spermatogonia and Sertoli cells, nor was there a remarkable difference in the estimated number of Leydig cells. Conclusion: The results indicate that even if there has been a deterioration in human semen quality, it is not necessarily caused by endocrine disruption of fetal testicular development. (Reprod Med Biol 2006; 5: 65-70).
Authors: R M Sharpe; N Atanassova; C McKinnell; P Parte; K J Turner; J S Fisher; J B Kerr; N P Groome; S Macpherson; M R Millar; P T Saunders Journal: Biol Reprod Date: 1998-11 Impact factor: 4.285
Authors: Karel De Gendt; Johannes V Swinnen; Philippa T K Saunders; Luc Schoonjans; Mieke Dewerchin; Ann Devos; Karen Tan; Nina Atanassova; Frank Claessens; Charlotte Lécureuil; Walter Heyns; Peter Carmeliet; Florian Guillou; Richard M Sharpe; Guido Verhoeven Journal: Proc Natl Acad Sci U S A Date: 2004-01-26 Impact factor: 11.205